Rapamycin activates TGF receptor independently of its ligand: implications for endothelial dysfunction

In conclusion, we provide evidence that rapamycin activates TGF receptor independent of its ligand TGFb, in concert with promotion of PAI-1 expression and changes in endothelial phenotype. These undesirable effects, the prothrombogenic state and activation of EndMT, are SMAD2-dependent and independent of the therapeutic rapamycin-induced cell proliferation arrest.

Source: Clinical Science - January 17, 2018 Category: Biomedical Science Authors: Miyakawa, A. A., Girao-Silva, T., Krieger, J. E., Edelman, E. R. Tags: PublishAheadOfPrint Source Type: research